Nicotine, Glioblastoma and Brain Tumours: The Research

Glioblastoma and other glioma cells carry nicotinic receptors, and laboratory studies have tested how nicotine and its metabolites affect their growth, invasion and response to chemotherapy. This page collects the published research on nicotine and brain tumours, each paper summarised in plain language with its PubMed record.

This collection is research only: papers found on PubMed, each described as its own abstract reports it. Cell and animal results are labelled as such, and harms are listed beside benefits. It is not medical advice.

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The Papers (8)

Newest first. Study types on this page — Review: 1 · Animal study: 1 · Cell study: 5 · Other: 1. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Investigating the potential risk of nicotine exposure on glioblastoma: Integrating Mendelian randomization and network toxicology analysis

Other, 2026. This study used only computer and database analyses to ask whether nicotine exposure might be linked to glioblastoma, an aggressive brain cancer. It used a genetic method called Mendelian randomization to look at genetically predicted blood levels of cotinine, which the body makes from nicotine, and reported a causal link between cotinine and glioblastoma. Database searches found 194 genes that nicotine might affect, involved in viral infection, immunity, cancer and metabolism, and narrowed these to six core genes, including NFκB1, HIF1α and MMP2. No patients, animals or cells were tested directly, and the authors present the results as new leads for future research on nicotine-related exposure and glioblastoma risk.

Yu S, Long M, Huang N et al. (2026). Investigating the potential risk of nicotine exposure on glioblastoma: Integrating Mendelian randomization and network toxicology analysis. Comput Biol Chem. — PubMed PMID: 41967427 · doi:10.1016/j.compbiolchem.2026.109061

The Distinct Biological Effects of 6-Hydroxy-L-Nicotine in Representative Cancer Cell Lines

Cell study, 2024. Researchers tested 6-hydroxy-L-nicotine, a compound made from nicotine, on three kinds of cancer cells grown in the lab (lung, breast and brain-tumour cells) and on two kinds of normal lung and breast cells. Computer modelling suggested the compound may bind to nicotinic receptors, the same receptor family nicotine acts on. In the lab dishes it made the brain-tumour (glioblastoma) cells grow more, held back the breast cancer cells, and had no effect on the lung cancer cells. The normal cells stayed alive at the same rate, but all of these results come from cells in dishes and computer models, not from animals or people.

Postu PA, Boiangiu RS, Mihasan M et al. (2024). The Distinct Biological Effects of 6-Hydroxy-L-Nicotine in Representative Cancer Cell Lines. Molecules. — PubMed PMID: 39683752 · doi:10.3390/molecules29235593

Choline and nicotine increase glioblastoma cell proliferation by binding and activating α7- and α9- containing nicotinic receptors

Cell study, 2021. Researchers tested whether nicotine and choline affect glioblastoma, the most common and most aggressive type of brain tumour that starts in the brain. They used two lines of human glioblastoma cells grown in the lab, one of them resistant to the chemotherapy drug temozolomide. Both nicotine and choline made the tumour cells multiply faster and switched on cell pathways that help cells grow and avoid dying. These effects went away when the alpha-7 or alpha-9 nicotinic receptors were blocked or switched off. Because these results come only from cells in a dish, the authors suggest these receptors might play a part in how aggressive the tumour is and could become targets for new treatments.

Pucci S, Fasoli F, Moretti M et al. (2021). Choline and nicotine increase glioblastoma cell proliferation by binding and activating α7- and α9- containing nicotinic receptors. Pharmacol Res. — PubMed PMID: 33276105 · doi:10.1016/j.phrs.2020.105336

Nicotine does not affect stem cell properties requisite for suicide gene therapy against glioma

Cell study, 2020. Researchers wanted to know whether nicotine might interfere with an experimental brain-tumor treatment that uses stem cells to carry tumor-killing genes to glioma cells. They tested mouse neural stem cells and human stem cells from dental pulp in laboratory dishes, at nicotine levels that did not kill cells, including a level described as similar to habitual smoking. Nicotine did not change how well the stem cells moved toward the tumor cells, and it did not change how the stem cells and tumor cells passed signals to each other through direct cell-to-cell connections. These results come only from cells grown in the laboratory, not from animals or people.

Kenmochi H, Yamasaki T, Koizumi S et al. (2020). Nicotine does not affect stem cell properties requisite for suicide gene therapy against glioma. Neurol Res. — PubMed PMID: 32588772 · doi:10.1080/01616412.2020.1782123

Potential effects of nicotine on glioblastoma and chemoradiotherapy: a review

Review, 2019. This review looked at how nicotine might affect glioblastoma, an aggressive brain cancer, and its treatment with radiation and chemotherapy. The authors note that about 16-28% of people with glioblastoma keep smoking after diagnosis and during treatment, and that published research on how smoking and nicotine affect glioblastoma care is sparse. Drawing on cell and tumor research, including studies of other cancers, they describe cell pathways that nicotine may act on to help the tumor grow and resist chemotherapy drugs. They conclude that understanding these effects should let doctors give patients with glioblastoma evidence-based advice about continuing to use nicotine-containing products during treatment.

McConnell DD, Carr SB, Litofsky NS (2019). Potential effects of nicotine on glioblastoma and chemoradiotherapy: a review. Expert Rev Neurother. — PubMed PMID: 31092064 · doi:10.1080/14737175.2019.1617701

Effect of Nicotine on CYP2B1 Expression in a Glioma Animal Model and Analysis of CYP2B6 Expression in Pediatric Gliomas

Animal study, 2018. Cyclophosphamide is a chemotherapy drug used for brain tumors called gliomas, and it has to be switched on by a liver-type enzyme (CYP2B6 in people, CYP2B1 in rats) before it works. In rats, researchers tested whether nicotine raises the level of this enzyme. Nicotine raised the enzyme in the brain tissue of healthy rats. In rats with glioma, the tumor already had high levels before treatment, and nicotine did not raise them much further inside the tumor, but did raise them in the tissue around it, especially near blood vessels. The researchers also measured the human enzyme in tumor samples from children with glioma and found that levels varied, possibly with how aggressive the tumor was. They suggest that raising the enzyme in tumors that have low levels could be a way to make the chemotherapy work better, but the nicotine results come only from rats.

Nava-Salazar S, Gómez-Manzo S, Marcial-Quino J et al. (2018). Effect of Nicotine on CYP2B1 Expression in a Glioma Animal Model and Analysis of CYP2B6 Expression in Pediatric Gliomas. Int J Mol Sci. — PubMed PMID: 29914177 · doi:10.3390/ijms19061790

Nicotine enhances proliferation, migration, and radioresistance of human malignant glioma cells through EGFR activation

Cell study, 2013. Researchers tested nicotine on two lines of human brain tumor (malignant glioma) cells grown in the lab. At levels similar to those found in long-term smokers, nicotine made the tumor cells grow, move and form colonies more, and made them more resistant to radiation treatment. Nicotine switched on a growth-signaling receptor called EGFR and the AKT and ERK pathways downstream of it, and drugs that block these pathways reduced the effects. These results come only from cells in a dish, not from animals or people.

Khalil AA, Jameson MJ, Broaddus WC et al. (2013). Nicotine enhances proliferation, migration, and radioresistance of human malignant glioma cells through EGFR activation. Brain Tumor Pathol. — PubMed PMID: 22614999 · doi:10.1007/s10014-012-0101-5

Calcium mobilization during nicotine-induced cell death in human glioma and glioblastoma cell lines

Cell study, 1998. Researchers exposed three human brain tumor cell lines (one glioma and two glioblastoma lines) to nicotine in the laboratory. Nicotine killed the tumor cells, and higher doses killed more of them. It did not break up their DNA in the pattern seen when leukemia cells die by programmed cell death. Nicotine quickly raised calcium levels inside the cells, more in the nucleus than in the rest of the cell, and the authors suggest this build-up of calcium in the nucleus is an important early step in nicotine-induced cell death. These results come only from cells grown in the lab, not from people or animals.

Yamamura M, Amano Y, Sakagami H et al. (1998). Calcium mobilization during nicotine-induced cell death in human glioma and glioblastoma cell lines. Anticancer Res. — PubMed PMID: 9703899

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